DOCSLIB.ORG

Corticosteroid Treatment, Serum Lipids and Coronary Artery Disease D. B. JEFFERYS M

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Corticosteroid Treatment, Serum Lipids and Coronary Artery Disease D. B. JEFFERYS M Postgrad Med J: first published as 10.1136/pgmj.56.657.491 on 1 July 1980. Downloaded from Postgraduate Medical Journal (July 1980) 56, 491-493 Corticosteroid treatment, serum lipids and coronary artery disease D. B. JEFFERYS M. H. LESSOF B.Sc., M.R.C.P. M.D., F.R.C.P. M. B. MATTOCK Ph.D. Department of Medicine, Guy's Hospital, London Bridge SE] 9RT Summary cholesterol out of the tissue and back into the general Serum lipids and the cholesterol concentrations in the metabolic pool, where it may be catabolized. high density lipoprotein (HDL) fractions were meas- In this study the authors have looked at the long- ured in patients receiving long-term corticosteroid term effects of corticosteroids on HDL cholesterol. treatment for connective tissue disorders and asthma. They have studied 3 groups: patients who are receiv- Patients who were not receiving corticosteroid ing corticosteroids; age-, sex- and disease-matched treatment had blood lipid levels which did not differ patients who are not receiving such treatment; and from those of healthy people. However, female (but healthy age- and sex-matched controls. not male) patients who had received prednisolone for a mean period of 3-1 years had a significant elevation Patients and methods in total cholesterol and a large decrease in HDL Subjects cholesterol. It seems possible that high levels of The serum total cholesterol, triglycerides and copyright. corticosteroids may increase the incidence of pre- HDL cholesterol were measured for 16 pre-meno- menopausal ischaemic heart disease in females. pausal female patients (age range 18-34 years) and 15 males (ages 24-38 years) who were all receiving Introduction long-term corticosteroid treatment. The body weights Corticosteroids are frequently used in the long- were all within 5% of the predicted weight from term management of connective tissue disorders and standardized life assurance tables. Three of the occasionally in patients with asthma and sarcoid. females were taking an oral contraceptive, whilst http://pmj.bmj.com/ In addition to the traditional complications of this only 2 of the males and none of the females were treatment, Kalbak (1972) showed an increase in cigarette smokers. None had a known family history peripheral atherosclerosis during corticosteroid ofhyperlipidaemia. The average dose of prednisolone treatment for rheumatoid arthritis. As compared to was 17-0 mg/day for the females and 17-2 mg for the well matched controls, Bulkley and Roberts (1975) males. The mean duration of treatment was 3-1 found an increased incidence of coronary athero- years for the females and 3-4 years for the males. sclerosis at post-mortem in 36 patients who had The patients studied were all in remission from received corticosteroids for a variety of conditions their disease at the time of investigation. This was on September 24, 2021 by guest. Protected including systemic lupus and rheumatoid arthritis. judged from clinical impression and from sedi- An increased incidence of coronary artery disease mentation rates, biochemical profiles and respiratory has also come to be recognized in renal transplant function tests. patients on corticosteroids (Evans and Ghosh, Three of the patients with Behret's syndrome 1979). were taking azathioprine 50 mg twice/day, one of the The mechanism for this accelerated atherosclerosis rheumatoids was taking naproxen 200 mg thrice/day is unclear. El-Shaboury and Hayes (1973) showed and one patient with urticarial vasculitis was receiving that both triglycerides and cholesterol were increased cimetidine 400 mg at night. Apart from the asthma- in 100 female asthmatics on long-term corticosteroid tics, who were using bronchodilator aerosols, the treatment. Current interest in lipid metabolism steroid patients were on no other regular medica- centres on the high density lipoproteins and their tions. In the control group 3 patients were taking inverse relationship to ischaemic heart disease azathioprine 100 mg daily. (Gordon et al., 1977). These levels may be parti- The conditions for which they were receiving cularly significant if, as has been suggested, high prednisolone were mainly connective tissue disorders, density lipoproteins are responsible for transferring including Behget's syndrome (13), systemic lupus 0032-5473/80/0700-0491 $02.00 © 1980 The Fellowship of Postgraduate Medicine Postgrad Med J: first published as 10.1136/pgmj.56.657.491 on 1 July 1980. Downloaded from 492 D. B. Jefferys, M. H. Lessof and M. B. Mattock (2), rheumatoid arthritis (4), polyarteritis (2), to HDL ratio is one of the most sensitive predictors urticarial vasculitis (2), sarcoidosis (4) and asthma of coronary artery disease (Miller et al., 1977). (4). The blood samples were taken after a 14-hr In such studies, pre-menopausal women have higher fast. HDL cholesterol concentrations. From the authors' observation, long-term corticosteroid treatment Methods appears to reverse the usual pre-menopausal The fasting serum triglyceride and cholesterol pattern of HDL cholesterol. Indeed, by generally concentrations and the cholesterol concentrations accepted criteria young female patients in this study of the high density lipoprotein (HDL) fractions were were likely to have a considerably increased risk assayed by standard Technicon Autoanalyser II of premature coronary artery disease. In keeping enzymatic methods. with this, 2 of the female patients have a history of The HDL fraction was measured in the super- angina pectoris with exercise ECG changes. They natant following specific precipitation from serum had no family history of ischaemic heart disease. of very low density and low density lipoproteins It was felt important to exclude a primary effect by sodium phosphotungstate and magnesium of the disease on the serum lipid concentrations, or chloride (Lopes Virella, Stone and Colwell, 1977). the influence of other drugs on lipid metabolism. It has been confirmed that this method shows good The patients studied were all young and were in agreement with a reference ultracentrifugal technique remission from their various diseases at the time of of HDL separation (Mattock et al., 1979). investigation. Many had been referred for an opinion as to whether their corticosteroids could be Results reduced or steroid-sparing drugs introduced. The There was no significant difference between the study was designed to compare the patients on disease-, age- and sex-matched controls, compared steroids with disease-matched controls and healthy to the healthy controls, in any of the serum lipids subjects. This was facilitated by the fact that the (Table 1). A notable difference was found between authors were simultaneously looking at a large the male and female patients receiving cortico- group of patients with Behcet's syndrome (Lessof steroids. The male patients had lower levels of et al., 1979). It could be argued that either thecopyright. triglycerides and total cholesterol. They had connective tissue disease, or additional drug therapy, significantly higher levels of HDL cholesterol and such as immunosuppressives, would alter the blood of the total cholesterol to HDL cholesterol ratio lipids. In fact only 3 patients were receiving, or had (P<0001). Thus long-term corticosteroids appear received, azathioprine in addition to the cortico- to reverse the usual higher HDL levels seen in steroids. Three similar patients on azathioprine females. were therefore included in the disease-matched control group. Since the patients were in remission Discussion it was possible to establish well matched controls. http://pmj.bmj.com/ The principal finding of this study was the Several of the patients were on inappropriately high marked sex difference in the effect of long-term doses of steroids and these were subsequently corticosteroid administration on HDL cholesterol. reduced without ill effect. Epidemiological studies of ischaemic heart disease Attention was also paid to the other factors which have shown that there is an inverse relationship are known to influence HDL concentrations. with HDL cholesterol and that the cholesterol Obesity, cigarette smoking and alcohol consumption on September 24, 2021 by guest. Protected TABLE 1. Results Serum lipids and high density lipoprotein (HDL) cholesterol all in mmol/l (+s.d.) Corticosteroid Disease-matched Healthy Significance, controls Group group controls controls v. steroid group Total triglycerides Male (n= 15) 1-21 (0-42) 0 90 (0-21) 0-87 (0 56) NS (mmol/l) Female (n= 16) 1-84 (0 55) 0 91 (0 29) 0 90 (0-28) P<0-05 Total cholesterol Male 5-61 (0 28) 5 33 (0-31) 5 28 (0 15) NS (mmol/1) Female 6 58 (1-04) 4-81 (0-81) 4-93 (0-57) P<0-05 HDL cholesterol Male 1-40 (0-31) 1-54 (0 15) 1 50 (0-53) NS (mmol/l) Female 1-10 (0-26) 1 99 (0-25) 1-78 (0 35) P<0-01 Ratio of Total cholesterol Male 4 00 3-46 3-71 NS HDL cholesterol Female 5 98 2-42 2-78 P<0-001 Postgrad Med J: first published as 10.1136/pgmj.56.657.491 on 1 July 1980. Downloaded from Corticosteroid treatment and coronary heart disease 493 were found to be similar within the groups. No disease in itself and, particularly in female patients, glucose intolerance was noted. Three of the female should be kept to a minimum. patients were taking oral contraceptives but their HDL cholesterol levels were in the range seen in other female patients. It was therefore concluded that the sex difference in HDL concentration was References BULKLEY, B.H. & ROBERTS, W.C. (1975) The heart in systemic attributable to the corticosteroid treatment rather lupus erythematosus and the changes induced in it by than to the disease or to other therapy. corticosteroid therapy. American Journal of Medicine, 58, The accelerated atherosclerosis seen in patients on 243. corticosteroids has been above. EL-SHABOURY, A.H. & HAYES, T.M. (1973) Hyperlipidaemia long-term quoted in asthmatic patients receiving long-term steroid therapy.
Load more

Recommended publications
  • Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses
    life Review Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses Inseok Choi , Hyewon Son and Jea-Hyun Baek * School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; [email protected] (I.C.); [email protected] (H.S.) * Correspondence: [email protected]; Tel.: +82-54-260-1347 Abstract: The tricarboxylic acid cycle (TCA) is a series of chemical reactions used in aerobic organisms to generate energy via the oxidation of acetylcoenzyme A (CoA) derived from carbohydrates, fatty acids and proteins. In the eukaryotic system, the TCA cycle occurs completely in mitochondria, while the intermediates of the TCA cycle are retained inside mitochondria due to their polarity and hydrophilicity. Under cell stress conditions, mitochondria can become disrupted and release their contents, which act as danger signals in the cytosol. Of note, the TCA cycle intermediates may also leak from dysfunctioning mitochondria and regulate cellular processes. Increasing evidence shows that the metabolites of the TCA cycle are substantially involved in the regulation of immune responses. In this review, we aimed to provide a comprehensive systematic overview of the molecular mechanisms of each TCA cycle intermediate that may play key roles in regulating cellular immunity in cell stress and discuss its implication for immune activation and suppression. Keywords: Krebs cycle; tricarboxylic acid cycle; cellular immunity; immunometabolism 1. Introduction The tricarboxylic acid cycle (TCA, also known as the Krebs cycle or the citric acid Citation: Choi, I.; Son, H.; Baek, J.-H. Tricarboxylic Acid (TCA) Cycle cycle) is a series of chemical reactions used in aerobic organisms (pro- and eukaryotes) to Intermediates: Regulators of Immune generate energy via the oxidation of acetyl-coenzyme A (CoA) derived from carbohydrates, Responses.
    [Show full text]
  • Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I
    Handout 5 Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I. Overall concepts A. Definitions 1. De novo synthesis = synthesis from non-fatty acid precursors a. Carbohydrate precursors (glucose and lactate) 1) De novo fatty acid synthesis uses glucose absorbed from the diet rather than glucose synthesized by the liver. 2) De novo fatty acid synthesis uses lactate derived primarily from glucose metabolism in muscle and red blood cells. b. Amino acid precursors (e.g., alanine, branched-chain amino acids) 1) De novo fatty acid synthesis from amino acids is especially important during times of excess protein intake. 2) Use of amino acids for fatty acid synthesis may result in nitrogen overload (e.g., the Atkins diet). c. Short-chain organic acids (e.g., acetate, butyrate, and propionate) 1) The rumen of ruminants is a major site of short-chain fatty acid synthesis. 2) Only small amounts of acetate circulate in non-ruminants. 2. Lipogenesis = fatty acid or triacylglycerol synthesis a. From preformed fatty acids (from diet or de novo fatty acid synthesis) b. Requires source of carbon (from glucose or lactate) for glycerol backbone 3T3-L1 Preadipocytes at confluence. No lipid 3T3-L1 Adipocytes after 6 days of filling has yet occurred. differentiation. Dark spots are lipid droplets. 1 Handout 5 Fatty Acid Synthesis B. Tissue sites of de novo fatty acid biosynthesis 1. Liver. In birds, fish, humans, and rodents (approx. 50% of fatty acid biosynthesis). 2. Adipose tissue. All livestock species synthesize fatty acids in adipose tissue; rodents synthesize about 50% of their fatty acids in adipose tissue.
    [Show full text]
  • Lipid Metabolism
    Objectives By the end of lecture the student should: Discuss β oxidation of fatty acids. Illustrate α oxidation of fatty acids. Understand ω oxidation of fatty acids. List sources and fates of active acetate. Oxidation of Fatty Acids 1- β-Oxidation (knoop’s oxidation): . Removal of 2 carbon fragment at a time form Acyl CoA (active FA). .The 2 carbon removed as acetyl CoA. .It occurs in many tissues including liver, kidney & heart FAs to be oxidized must be entered the following 2 steps 2- Transport of acyl 1-Activation of FA COA to mitochondria 1-FA activation Acyl COA synthetase RCOOH RCO~SCOA COASH ATP AMP+P~P 2Pi + E Pyrophosphatase 2- Transport of acyl COA to mitochondria: . Role of carnitine in the transport of LCFA through the inner mithochochondrial membrane Functions of carnitine 1- Transport long chain acyl COA across mitochondrial membrane into the mitochondria so it increases the rate of oxidation of LCFA 2- Transport acetyl-CoA from mitochondria to cytoplasm So it stimulates fatty acid synthesis CoA CoA--SHSH H C α H3C3 α β Cβ Palmitoyl Palmitoyl-CoA -CoA β O ~ S – CoA α H3C α H3C β β CO CO ~ S~ –S CoA – CoA β + + CH3 – CO ~ S –CoA Successive removal of C2 units Acetyl-CoA 8CH3 – CO ~ S – CoA 8CH3 – CO ~ S –Acetyl CoA-CoA Acetyl-CoA Steps of β- Oxidation of FAs Energetics of FA oxidation Palmitic (16C): . β-oxidation of palmitic acid will be repeated 7 cycles producing 8 molecules of acetyl COA . In each cycle FADH2 and NADH+H+ is produced & transported to respiratory chain FADH2 ------------------ 2 ATP NADH+H+ ------------- 3 ATP So 7 cycles 5X7=35 ATP .
    [Show full text]
  • Regulation of Ketone Body and Coenzyme a Metabolism in Liver
    REGULATION OF KETONE BODY AND COENZYME A METABOLISM IN LIVER by SHUANG DENG Submitted in partial fulfillment of the requirements For the Degree of Doctor of Philosophy Dissertation Adviser: Henri Brunengraber, M.D., Ph.D. Department of Nutrition CASE WESTERN RESERVE UNIVERSITY August, 2011 SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of __________________ Shuang Deng ____________ _ _ candidate for the ________________________________degree Doctor of Philosophy *. (signed) ________________________________________________ Edith Lerner, PhD (chair of the committee) ________________________________________________ Henri Brunengraber, MD, PhD ________________________________________________ Colleen Croniger, PhD ________________________________________________ Paul Ernsberger, PhD ________________________________________________ Janos Kerner, PhD ________________________________________________ Michelle Puchowicz, PhD (date) _______________________June 23, 2011 *We also certify that written approval has been obtained for any proprietary material contained therein. I dedicate this work to my parents, my son and my husband TABLE OF CONTENTS Table of Contents…………………………………………………………………. iv List of Tables………………………………………………………………………. viii List of Figures……………………………………………………………………… ix Acknowledgements………………………………………………………………. xii List of Abbreviations………………………………………………………………. xiv Abstract…………………………………………………………………………….. xvii CHAPTER 1: KETONE BODY METABOLISM 1.1 Overview……………………………………………………………………….. 1 1.1.1 General introduction
    [Show full text]
  • CHAPTER-IV LIPID METABOLISM BETA-OXIDATION Beta-Oxidation Is
    CHAPTER-IV LIPID METABOLISM BETA-OXIDATION Beta-oxidation is the process by which fatty acids, in the form of acyl-CoA molecules, are broken down in mitochondria and/or peroxisomes to generate acetyl-CoA, the entry molecule for the citric acid cycle. The beta oxidation of fatty acids involve three stages: 1. Activation of fatty acids in the cytosol 2. Transport of activated fatty acids into mitochondria (carnitine shuttle) 3. Beta oxidation proper in the mitochondrial matrix Fatty acids are oxidized by most of the tissues in the body. However, some tissues such as the adrenal medulla do not use fatty acids for their energy requirements and instead use carbohydrates. Energy yield The ATP yield for every oxidation cycle is 14 ATP (according to the P/O ratio), broken down as follows: Source ATP Total [citation needed] 1 FADH2 x 1.5 ATP = 1.5 ATP (some sources say 2 ATP) 1 NADH x 2.5 ATP = 2.5 ATP (some sources say 3 ATP) 1 acetyl CoA x 10 ATP = 10 ATP (some sources say 12 ATP) TOTAL = 14 ATP For an even-numbered saturated fat (C2n), n - 1 oxidations are necessary, and the final process yields an additional acetyl CoA. In addition, two equivalents of ATP are lost during the activation of the fatty acid. Therefore, the total ATP yield can be stated as: (n - 1) * 14 + 10 - 2 = total ATP For instance, the ATP yield of palmitate (C16, n = 8) is: (8 - 1) * 14 + 10 - 2 = 106 ATP Represented in table form: Source ATP Total 7 FADH2 x 1.5 ATP = 10.5 ATP 7 NADH x 2.5 ATP = 17.5 ATP 8 acetyl CoA x 10 ATP = 80 ATP Activation = -2 ATP NET = 106 ATP For sources that use the larger ATP production numbers described above, the total would be 129 ATP ={(8-1)*17+12-2} equivalents per palmitate.
    [Show full text]
  • Lipid and Carbohydrate Metabolism in Caenorhabditis Elegans
    | WORMBOOK METABOLISM, PHYSIOLOGY, AND AGING Lipid and Carbohydrate Metabolism in Caenorhabditis elegans Jennifer L. Watts*,1 and Michael Ristow† *School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, Washington 99164 and †Energy Metabolism Laboratory, Institute of Translational Medicine, Department of Health Sciences and Technology, Swiss Federal Institute of Technology Zurich, 8603 Schwerzenbach-Zurich, Switzerland ORCID ID: 0000-0003-4349-0639 (J.L.W.) ABSTRACT Lipid and carbohydrate metabolism are highly conserved processes that affect nearly all aspects of organismal biology. Caenorhabditis elegans eat bacteria, which consist of lipids, carbohydrates, and proteins that are broken down during digestion into fatty acids, simple sugars, and amino acid precursors. With these nutrients, C. elegans synthesizes a wide range of metabolites that are required for development and behavior. In this review, we outline lipid and carbohydrate structures as well as biosynthesis and breakdown pathways that have been characterized in C. elegans. We bring attention to functional studies using mutant strains that reveal physiological roles for specific lipids and carbohydrates during development, aging, and adaptation to changing environmental conditions. KEYWORDS Caenorhabditis elegans; ascarosides; glucose; fatty acids; phospholipids; sphingolipids; triacylglycerols; cholesterol; maradolipids; WormBook TABLE OF CONTENTS Abstract 413 Fatty Acids 415 Characteristics of C. elegans fatty acids 415 Methods
    [Show full text]
  • Lipid Metabolism & Obesity
    ™ Proteome Profi ler Mouse Obesity Array Kit PRSRT STD R&D Systems Proteome Profi ler Antibody Arrays offer a rapid, sensitive approach to simultaneously detect the relative levels of multiple analytes in U.S. POSTAGE R&D Systems Tools for Cell Biology Research™ a single sample. Each array is designed using carefully selected capture antibodies that are spotted in duplicate onto nitrocellulose membranes. PAID Membranes are incubated with experimental samples containing the proteins of interest and a cocktail of biotinylated detection antibodies. R&D SYSTEMS Streptavidin-HRP and chemiluminescent detection reagents are subsequently added to produce a signal that is proportional to the amount of R&D Systems, Inc. 614 McKinley Place NE analyte bound. The use of these arrays requires no specialized equipment and eliminates the need to perform multiple immunoprecipitation/ Minneapolis, MN 55413 Western blot experiments. TEL: (800) 343-7475 (612) 379-2956 ABUndifferentiated C FAX: (612) 656-4400 Mouse Obesity Array (Catalog # ARY013) www.RnDSystems.com Adiponectin IGFBP-3 Leptin IGF-I 70,000 Contains 4 membranes - each spotted in duplicate with 38 different obesity-related antibodies 60,000 • Adiponectin/Acrp30 • IGFBP-2 • Pentraxin 3 50,000 • AgRP • IGFBP-3 • Pref-1/DLK-1/FA1 Lipid Metabolism & Obesity • ANGPT-L3 • IGFBP-5 • RAGE 40,000 VEGF Pentraxin 3 Resistin Lipocalin-2 • CRP • IGFBP-6 • RANTES/CCL5 • DPPIV • IL-6 • RBP4 Pixel Density Pixel 30,000 • Endocan • IL-10 • Resistin Differentiated 20,000 • Fetuin A • IL-11 • Serpin E1/PAI-1 10,000 • FGF acidic/FGF-1 • Leptin • TIMP-1 Adiponectin IGFBP-3 Leptin IGF-I • FGF-21 • LIF • TNF- 0 • HGF • Lipocalin-2/NGAL • VEGF IGF-I VEGF • ICAM-1/CD54 • MCP-1 Leptin Resistin IGFBP-3 • IGF-I • M-CSF Lipocalin-2 Pentraxin 3 Pentraxin Adiponectin Printed on recyclable paper • IGF-II • Oncostatin M 10% post consumer waste.
    [Show full text]
  • The Citric Acid Cycle
    BI/CH 422/622 Announcements: Exam 1 is TONIGHT in Morse at 7:00 pm OUTLINE: Glycogenolysis Glycolysis Introduction & overview; 2 phases Phase I Phase II Summary: logic, energetics, labeling studies Other sugars Pasteur: Anaerobic vs Aerobic Fermentations Lactate-lactate dehydrogenase Exam-1 material Ethanol-pyruvate decarboxylase & alcohol dehydrogenase Acetoacetate decarboxylase Pyruvate pyruvate dehydrogenase Krebs’ Cycle How did he figure it out? Overview 8 Steps Citrate Synthase Pyruvate Oxidation Enzyme 1 • Step 1: Decarboxylation of pyruvate to an enol (hydroxyethyl-TPPl • Step 2: Acylation of enol to a thioester on lipoic acid. Enzyme 2 • Step 3: Formation of acetyl-CoA: simple thio-ester exchange Enzyme 3 • Step 4: Reoxidation of the lipoamide cofactor; reduction of FAD/Cys/Cys • Step 5: Regeneration of the oxidized FAD/Cys/Cys active site – forming NADH 1 Pyruvate Oxidation E196, E224, E324 E2 Pyruvate Oxidation E196, E224, E324 E2 2 Pyruvate Oxidation Overall Reaction of PDC Pyruvate + Coenzyme-A (CoASH) + NAD+ ⇌ PDC (TPP, lipoic acid, FAD) DG°’ = –8 kcal/mol + CO2 + Acetyl-Coenzyme-A (Ac-CoA) + NADH + H Fates of Acetyl CoA (HMG-CoA) Amino acids 1. Oxidation 2. Lipid metabolism 3. Amino acid metabolism Pyruvate Oxidation Overall Reaction of PDC Pyruvate + Coenzyme-A (CoASH) + NAD+ ⇌ PDC (TPP, lipoic acid, FAD) DG°’ = –8 kcal/mol + CO2 + Acetyl-Coenzyme-A (Ac-CoA) + NADH + H Fates of Acetyl CoA (HMG-CoA) Amino acids 1. Oxidation 2. Lipid metabolism 3. Amino acid metabolism 3 The Citric Acid Cycle Glycogen-o-lysis Glyco-lysis Pyruvate Oxidation Krebs' Cycle Phosphorylation Oxidative The Citric Acid Cycle a.k.a. Krebs Cycle, a.k.a.
    [Show full text]
  • Lipid Metabolism Course Code: ZOOL 4008 (Biochemistry and Metabolism) M.Sc
    Lipid Metabolism Course Code: ZOOL 4008 (Biochemistry and Metabolism) M.Sc. (Zoology), Semester –II Dr. Shyam Babu Prasad Assistant Professor Department of Zoology Mahatma Gandhi Central University (MGCU), Motihari-845401 (Bihar) Email: [email protected] Lipids •A lipids are non-polar organic compounds that is insoluble in water and soluble in alcohol, ether, and chloroform. •Lipids are an important constituent of the structure of living cells. Together with carbohydrates and proteins, lipids are the main constituents of plant and animal cells. •Lipids are easily stored in the body and serve as a source of Energy/Fuel. •Lipids includes fatty acids, neutral fats, waxes and steroids (like cortisone) etc. Almost all fat in your diet comes in the form of triglycerides •Fatty acids rarely occur as free molecules in nature. it is found in complex molecules such as fats (energy-storage compounds) and phospholipids (the primary lipid components of cellular membranes). Lipids Classification Simple Lipids: Complex Lipids: Precursor and Esters of fatty acids Esters of fatty acids with derived Lipids: various alcohols + Other with various alcohols. Steroids, other Groups like phosphoric They are Saturated and alcohols, fatty acids, sugar residue etc. Unsaturated aldehydes, and ketone for ex. (Ex. Fats, oil and bodies, lipid-soluble Waxes) A. Phospholipids (glycerophospholipid vitamins, and s and hormones. sphingophospholipid s ) B. Glycolipids (glycosphingolipids) : Carbohydrates containing lipids. C. Other complex lipids: Sulfolipids, aminolipids, and Lipoproteins. Structure of Lipids Fatty acids are composed of a hydrocarbon chain with one terminal carboxyl group (COOH). At physiological condition hydrogen ion (H+) lost to form a negatively charged carboxylate group (COO−).
    [Show full text]
  • Disorders of Lipid Metabolism Disorders of Lipid Metabolism (DLM) Guideline (2011)
    Disorders of Lipid Metabolism Disorders of Lipid Metabolism (DLM) Guideline (2011) Disorders of Lipid Metabolism DLM: Introduction (2011) Guideline Title Disorders of Lipid Metabolism (2011) Evidence-Based Nutrition Practice Guideline Guideline Narrative Overview This guideline updates the 2005 ADA Disorders of Lipid Metabolism Evidence-based Nutrition Practice Guideline. The objective of the Disorders of Lipid Metabolism (DLM) guidelines is to provide Medical Nutrition Therapy (MNT) guideline recommendations that support improvement in lipid levels and risk factor management of cardiovascular disease (CVD). The focus of this guideline is on the treatment of lipid metabolism disorders - that is, patients with elevated low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), or triglyceride (TG) levels, and low high-density lipoprotein cholesterol (HDL-C) levels, as well as coronary health issues such as metabolic syndrome and hypertension (HTN). Disorders of Lipid Metabolism are recognized risk factors for atherosclerotic diseases, including coronary heart disease (CHD). The relationship of TC and LDL-C subsequent to CHD events has been well documented in several major observational and clinical studies.1 An increasing body of evidence links dyslipidemias to the occurrence of stroke.2 Clinical trials have found that lowering LDL-C lowers coronary events. Evidence is also accumulating that risk for CHD can be reduced beyond LDL-lowering therapy by modification of other risk factors. One potential secondary target of therapy is the metabolic syndrome, which represents a constellation of lipid and non-lipid risk factors of metabolic origin. National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III recognizes the metabolic syndrome as a secondary target of risk reduction therapy.3 This guideline includes metabolic syndrome management as a consideration.
    [Show full text]
  • The Regulation of Fat Metabolism During Aerobic Exercise
    biomolecules Review The Regulation of Fat Metabolism during Aerobic Exercise Antonella Muscella * , Erika Stefàno , Paola Lunetti *, Loredana Capobianco and Santo Marsigliante Department of Biological and Environmental Science and Technologies (Di.S.Te.B.A.), University of Salento, 73100 Lecce, Italy; [email protected] (E.S.); [email protected] (L.C.); [email protected] (S.M.) * Correspondence: [email protected] (A.M.); [email protected] (P.L.) Received: 3 November 2020; Accepted: 15 December 2020; Published: 21 December 2020 Abstract: Since the lipid profile is altered by physical activity, the study of lipid metabolism is a remarkable element in understanding if and how physical activity affects the health of both professional athletes and sedentary subjects. Although not fully defined, it has become clear that resistance exercise uses fat as an energy source. The fatty acid oxidation rate is the result of the following processes: (a) triglycerides lipolysis, most abundant in fat adipocytes and intramuscular triacylglycerol (IMTG) stores, (b) fatty acid transport from blood plasma to muscle sarcoplasm, (c) availability and hydrolysis rate of intramuscular triglycerides, and (d) transport of fatty acids through the mitochondrial membrane. In this review, we report some studies concerning the relationship between exercise and the aforementioned processes also in light of hormonal controls and molecular regulations within fat and skeletal muscle cells. Keywords: lipid metabolism;
    [Show full text]
  • Introduction of Lipid
    Usman Sumo Friend Tambunan Arli Aditya Parikesit Lumita Oktarin Ayu Puari Bioinformatics Grup Department of Chemistry Faculty of Mathematics and Science University of Indonesia The main functions of lipids › energy storage, › structural components of cell membranes, › as important signaling molecules. Oxidation of lipids produced more energy than the oxidation of carbohydrates. Humans have fat tissue under the skin, in the abdominal cavity, and in the mammary glands. Lipids cannot be digest directly. Lipids not easily accessible to digestive enzymes in aqueous phase. Dietary lipids have to emulsified first. Catabolism of fat (lipolysis) involves two separate pathways, glycerol pathway and fatty acids pathway. Glycerol Patyhway Glycerol with ATP converted into glycerol-3-phosphate by glycerol kinase and release one inorganic phosphate yields ADP. Then, it is oxidized by NAD+ into dihydroxyacetone- phosphate using glycerol-phosphate dehydrogenase. The oxidizing products entering glycolysis pathway and produced energy. Fatty Acid Pathway Fatty acid catabolism through beta oxidation (the broken down process of Acyl-CoA molecules into Acetyl-CoA) occurred in mitochondria and/or in peroxisomes. Beta oxditation will produced : Two-carbon acetic acid fragments, which are converted to acetyl-CoA and enter the Krebs cycle Reduced coenzymes, which are entered the electron transport chain An acetyl-CoA is then used in the Krebs Cycle to make one + + ATP , 3 NADH , H and 1 FADH2. If a fatty acid has 18 carbon units, then 9 acetyl CoA units would be made. Ketone Body Formation Low glucose levels in the blood causing ketogenesis. When it happened , oxaloacetate is depleted in liver because it is used for gluconeogenesis to get energy.
    [Show full text]